MUSCARINE RECEPTOR ACTIVATION IN THE SUBSTANTIA-GELATINOSA OF THE SPINAL TRIGEMINAL NUCLEUS OF THE GUINEA-PIG

1. Intracellular recordings were made from slices of guinea pig spinal trigeminal nucleus pars caudalis (SG). 2. Muscarine [0.3-30 mu M; hal f maximally effective concentration (EC(50)) = 2.9 mu M] hyperpolarize d 61% of SG neurons. The effect was mimicked by carbachol (0.3-30 mu M ; EC(50) = 3.9 mu M) and antagonized by pirenzepine (1 mu M). Thirty-f our percent of the neurons were depolarized by muscarine and carbachol (1-30 mu M; EC(50) = 5.7 mu M), and the effect was antagonized by pir enzepine (100 nM). 3. In similar to 80% of recordings, muscarine (10-3 0 mu M) evoked repetitive spontaneous inhibitory postsynaptic potentia ls (IPSPs) that were sensitive to bicuculline (10 mu M). 4. Muscarine (1-30 mu M; EC(50) = 3 mu M) decreased the amplitude of the majority o f evoked excitatory postsynaptic potentials (EPSPs), and the effect wa s mimicked by carbachol and antagonized by pirenzepine (100 nM). 5. Th ese results indicate that there are at least three mechanisms by which muscarine inhibits SG neurons: 1) hyperpolarization through activatio n of non-MI receptors; 2) activation of gamma-aminobutyric acid-contai ning interneurons that mediate IPSPs in a subset of neurons; and 3) a decrease in evoked EPSP amplitude. Muscarine can also activate SG neur ons via interaction with an MI-type receptor.